ArticleFuture microbiology2026
Targeting PPARγ-NF-κB: (+)-catechin reverses
Article in Future microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors.
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Abstract
background
methodsHuman colon epithelial Caco-2 cells were treated with TcdA to induce barrier dysfunction, followed by CC at varying concentrations. Barrier integrity was assessed using trans-epithelial electrical resistance (TEER), Lucifer yellow paracellular flux, and lactate dehydrogenase (LDH) release. The involvement of peroxisome proliferator-activated receptor gamma (PPARγ) and nuclear factor kappa B (NF-κB) signaling was evaluated using short hairpin RNA (shRNA)-mediated PPARγ knockdown.
resultsTcdA treatment disrupted Caco-2 barrier function, indicated by decreased TEER, increased Lucifer yellow flux, and elevated LDH release. TcdA treatment also reduced PPARγ expression and was associated with increased activation of the NF-κB signaling pathway. CC treatment significantly alleviated these effects in a concentration-dependent manner, with 100 μg/mL showing optimal protection. PPARγ knockdown partially attenuated the protective effects of CC and diminished its inhibitory effect on NF-κB activation, suggesting that PPARγ contributes to the barrier-protective role of CC.
conclusionCC attenuates TcdA-induced intestinal epithelial barrier dysfunction and is associated with modulation of the PPARγ-NF-κB signaling pathway.
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